Molecular analysis of TrkB:NMDA receptor interactions in the mouse brain

脑中神经细胞之间的细胞间通讯涉及突触前和突触后神经元之间的高度专门化的接触区域，称为突触。正是在这里，有一个丰富的受体和信号分子，响应神经递质和生长因子，反过来，可以加强和/或削弱一个特定的突触。特定突触的增加和/或丧失是称为神经元可塑性的过程的基础，并且正是该过程调节神经元活动以及学习和记忆的过程。两种不同类型的细胞表面受体已被证明在学习和记忆中发挥重要作用。首先，由大脑中的兴奋性神经递质激活的NMDA受体（例如，谷氨酸）和第二，称为TrkB的受体，其响应称为脑源性神经营养因子（BDNF）的生长因子。由于这是两种非常不同类型的受体，因此尚不清楚它们如何共同调节这一过程。

Intercellular communication between nerve cells in the brain involves highly specialized regions of contact,termed synapses, between pre and post-synaptic neurons. It is here that there is an enrichment of receptors and signaling molecules that respond to neurotransmitters and growth factors that, in turn, can strengthen and/or weaken a particular synapse. The increase and/or loss of particular synapses underlies a process termed neuronal plasticity and it is this process that modulates neuronal activity and the process of learning and memory. Two different classes of cell surface receptors have been shown to serve important roles in learning and memory. First, the NMDA receptors which are activated by excitatory neurotransmitters in the brain (eg. glutamate) and, second, a receptor termed TrkB which responds to a growth factor termed brain-derived neurotrophic factor (BDNF). Since these are 2 very different types of receptors, it is not well understood how they co-regulate this process.